Failure of mianserin to affect autonomic function in the pupils of depressed patients

Shur, Eric; Checkley, Stuart; Delgado, I.

doi:10.1111/j.1600-0447.1983.tb00330.x

Cited by 14 publications

(4 citation statements)

References 37 publications

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“…Responses to adrenergic agents did not distinguish groups. Dilsaver & Greden (50) concluded desipramine produced cholinergic system supersensitivity in depressed subjects. Twenty-one days of desipramine treatment, but not 7, produced enhancement of the miotic response to pilocarpine (51, 52).…”

Section: Pharmacological Perturbation Strategiesmentioning

confidence: 99%

“…The ability to establish correlations among clinical or phenomenological variables (mood, affect, psychomotor function, hedonia) (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), physiological measures (e.g., dexamethasone suppression test (DST) results, absolute post-dexamethasone plasma cortisol, l3-endorphin, and adrenocorticotropin hormone (ACTH) levels (32,33,(37)(38)(39)(40), polysomnographic parameters ( R E M latency and density, etc.) (41)(42)(43)(44)(45)(46)(47)(48), pupillometric data (49)(50)(51)(52), biochemical indices (phospholipid turnover, rate of cyclic GMP generation) (52-5 8 ) , and B,,,,,, and K,, for binding of muscarinic receptor ligands in viva (59-70) enhances experimental versatility. It also provides a powerful means of studying the same phenomenon from the multiple aspects which define or determine it.…”

Section: Pharmacological Perturbation Strategiesmentioning

confidence: 99%

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Cholinergic mechanisms in affective disorders

Dilsaver

1986

Acta Psychiatr Scand

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Advances in clinical and basic research methodology combined with clearly articulated concepts create new opportunities for researching the roles of cholinergic mechanisms in the pathophysiology of affective disorders. Areas for study include: roles of cholinergic mechanisms in mediating effects of stress and cholinergic mechanisms linking the pathophysiologies of affective and panic disorders, use of pharmacologic agents to produce cholinergic system supersensitivity in modeling biologic aspects of affective illness, use of multigenerational intrapedigree studies of cholinergic markers associated with affective disease, research into the neurobiology of lithium and ECT as they pertain to muscarinic cholinergic mechanisms, study of the interrelationship of sodium, calcium and lithium ion metabolism and their relationship to cholinergic-monoaminergic interaction, the development of brain imaging strategies and techniques, e.g., positron emission tomography (PET), to measure changes in cholinergic receptor density and affinity as a function of clinical state, identification and validation of a peripheral model of the central muscarinic receptor, study of the pharmacology of abusable substances and its relationship to mechanisms regulating mood, affect, psychomotor function and other variables related to the affective disorders, and development of in vitro and in vivo models useful in studying the physiology and biochemistry of the interaction of cholinergic and monoaminergic neurons. These models may allow us to bridge the traditional cholinergic and monoamine hypotheses of affective disorders.

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Section: Pharmacological Perturbation Strategiesmentioning

confidence: 99%

Section: Pharmacological Perturbation Strategiesmentioning

confidence: 99%

Cholinergic mechanisms in affective disorders

Dilsaver

1986

Acta Psychiatr Scand

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“…Additional data suggests that DMI produces cholinergic system supersensitivity in man and animals. Chronic treatment with DMI enhances the miotic response to pilocarpine in depressed subjects (Dilsaver and Greden, 1983;Shur et al, 1983). Nomura et al (1982b; reported that treatment with DMI, 10 zag/kg ip twice daily increases the negative ionotropic effects of acetylcholine and produces an exaggerated increase in the activity of ornithine decarboxylase in response to a cholinergic agonist.…”

Section: Mechanism Of Actionmentioning

confidence: 99%

Cholinergic properties of desipramine and amoxapine: Assessment using a thermoregulation paradigm

Dilsaver

Davidson

1987

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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1. The withdrawal of tricyclic antidepressants (TCAs) produces symptoms suggesting cholinergic rebound. 2. Amitriptyline (AMI), the most potent antimuscarinic agent among this class of drugs, produces supersensitivity to the muscarinic agonist, oxotremorine. 3. Enhancement of the sensitivity of cholinoceptive neurons to acetylcholine as a consequence of treatment with TCAs would account for many of the symptoms following the withdrawal of these drugs. 4. Desipramine (DMI) is the least potent antimuscarinic compound among the TCAs, yet its withdrawal produces withdrawal symptoms. 5. Recently, it was reported that amoxapine (AMX) weakly binds to muscarinic acetylcholine receptors (mAchR) in vitro. This may indicate that this drug lacks the effects antimuscarinic effects in vivo, and that it will not supersensitize cholinergic networks. 6. A thermoregulation paradigm was used to assess the sensitivity of a central muscarinic mechanism to oxotremorine before and after treatment with DMI and AMX. Treatment with either drug increased the hypothermic response to this agonist. 7. Mechanisms whereby drugs can produce cholinergic system supersensitivity, and the use of thermoregulation paradigms in assessing the properties of therapeutic agents is discussed.

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“…Changes in pupil diameter, in man, can be measured by a photographic method (Sneddon, 1968). Dose-response curves have been published for the miotic response to pilocarpine and the mydriatic response to phenylephrine (Shur et al, 1983) and to tyramine (Peet et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Effects of an alpha‐2 adrenoceptor antagonist, Org 3770, upon the autonomic function of the pupil

Palazidou

Sitsen

Checkley

1990

Human Psychopharmacology

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The effects of a single oral dose of an alpha-2 adrenoceptor antagonist, Org 3770 (30mg), upon the autonomic function of the human pupil have been investigated in six volunteers. Org 3770 reduced pupil diameter, possibly as a result of its alpha-2 adrenoceptor blocking activity. Org 3770 did not reduce the mydriatric effect of phenylephrine and tyramine, nor was the miotic response to pilocarpine affected. These results are consistent with a blockade by Org 3770 of central alpha-2 adrenoceptors.

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Failure of mianserin to affect autonomic function in the pupils of depressed patients

Cited by 14 publications

References 37 publications

Cholinergic mechanisms in affective disorders

Cholinergic mechanisms in affective disorders

Cholinergic properties of desipramine and amoxapine: Assessment using a thermoregulation paradigm

Effects of an alpha‐2 adrenoceptor antagonist, Org 3770, upon the autonomic function of the pupil

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